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通过足底皮下注射蝎毒BmK毒液诱导大鼠脊髓中c-Fos表达。

c-Fos expression in rat spinal cord induced by scorpion BmK venom via plantar subcutaneous injection.

作者信息

Bai Zhan-Tao, Chen Bing, Zhang Xu-Ying, Fan Guang-Li, Ji Yong-Hua

机构信息

Department of Biology of Yanan University, Yanan 716000, People's Republic of China.

出版信息

Neurosci Res. 2002 Dec;44(4):447-54. doi: 10.1016/s0168-0102(02)00177-3.

DOI:10.1016/s0168-0102(02)00177-3
PMID:12445632
Abstract

The aim of this study was to assess the cell-type and distribution of highly activated neurons in rat spinal cord underlying nociceptive responses induced by scorpion BmK venom using Fos immunohistochemistry. BmK venom was intraplantarly injected into one hind paw of a conscious rat. Fos-like immunoreactive neurons were found to predominantly distribute at L4-5 segments in the rat spinal cord after BmK venom application. c-Fos labeling was most dense in the medial half portion of laminae I-II, moderately dense in laminae V-VI and less dense in laminae III-IV, VII-X. c-Fos labeling could be detected at 0.5 h, reached the peak at 2 h, decreased steeply from 4 h and then almost disappeared at 24 h. Ten to fifty micrograms of BmK venom was deemed to be a sufficient dosage to evoke c-Fos expression. On the other hand, c-Fos expression induced by BmK venom could be suppressed partially by systemic morphine in a dose-dependent manner. The results suggest that the different extent of activities of neuronal subpopulation in the spinal cord involved in nociceptive transmission manifesting as c-Fos expression, were mainly correlated with mechanisms underlying the generation, maintenance and/or modulation of spontaneous pain and hyperalgesia evoked by BmK venom.

摘要

本研究旨在利用Fos免疫组织化学方法评估蝎毒BmK诱导大鼠伤害性反应时脊髓中高度激活神经元的细胞类型和分布。将BmK毒液经足底注射到清醒大鼠的一只后爪。应用BmK毒液后,发现Fos样免疫反应性神经元主要分布在大鼠脊髓的L4-5节段。c-Fos标记在I-II层的内侧半部最密集,在V-VI层中等密集,在III-IV层、VII-X层较稀疏。c-Fos标记在0.5小时可检测到,2小时达到峰值,4小时后急剧下降,24小时时几乎消失。10至50微克的BmK毒液被认为是诱发c-Fos表达的足够剂量。另一方面,BmK毒液诱导的c-Fos表达可被全身吗啡以剂量依赖性方式部分抑制。结果表明,脊髓中参与伤害性传递的神经元亚群活动程度不同,表现为c-Fos表达,主要与BmK毒液诱发的自发痛和痛觉过敏的产生、维持和/或调节机制相关。

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